1. REACTIVE ARTHRITIS

2. Definition
Reactive arthritis (ReA) refers to acute nonpurulent arthritis complicating an infection elsewhere in the body
In recent years, the term has been used primarily to refer to spondyloarthropathies following enteric or urogenital infections and occurring predominantly in individuals with the histocompatibility antigen HLA-B27

3. Reiter’s Syndrome
First reported in 1916 by Hans Reiter as a clinical triad of arthritis, nongonococcal urethritis, and conjunctivitis.
The definition of Reiter’s syndrome has been evolving. The term has been used interchangeably with “reactive arthritis,”
In 1981 the American Rheumatism Association defined the syndrome by the following criteria:
A peripheral arthritis lasting longer than one month associated with urethritis or cervicitis or diarrhea.

4. ETIOLOGY AND PATHOGENESIS
The first bacterial infection noted to be causally related to ReA was S. flexneri. An outbreak of shigellosis among Finnish troops in 1944 resulted in numerous cases of ReA

5. REACTIVE ARTHRITIS Postveneral:Chlamydia trachomatis
Postdysentric:Shigella, Salmonella, Yersinia, and Campylobacter, Clostridium difficile, Ureaplasma urealyticum

6. EPIDEMIOLOGY
ReA occurs predominantly in individuals who have inherited the B27 gene; in most series, 60 to 85% of patients are B27 positive
In epidemics of arthritogenic bacterial infection, e.g., S. flexneri, it has been estimated that ReA develops in ~20% of exposed B27-positive individuals

7. EPIDEMIOLOGY 18 to 40 years of age
sex ratio in ReA following enteric infection is nearly 1:1
whereas venereally acquired ReA is predominantly confined to men

8. PATHOLOGY
Synovial histology is similar to that of other inflammatory arthropathies
Enthesitis is a common clinical finding

9. ETIOLOGY AND PATHOGENESIS
Most, if not all, of the triggering organisms produce lipopolysaccharide (LPS) and share a capacity to attack mucosal surfaces, to invade host cells, and survive intracellularly

10. ETIOLOGY AND PATHOGENESIS
Antigens from Chlamydia, Yersinia, Salmonella, and Shigella have been shown to be present in the synovium and/or synovial fluid leukocytes of patients with ReA for long periods following the acute attack

11. ETIOLOGY AND PATHOGENESIS
T cells that specifically respond to antigens of the inciting organism are typically found in inflamed synovium but not in peripheral blood of patients with ReA
The role of HLA-B27 in ReA also remains to be determined

12. CLINICAL FEATURES
The clinical manifestations of ReA constitute a spectrum that ranges from an isolated, transient monarthritis to severe multisystem disease
Antecedent infection 1 to 4 weeks before the onset of symptoms
Constitutional symptoms are common

13. CLINICAL FEATURES
The musculoskeletal symptoms are usually acute in onse
Arthritis is usually asymmetric and additive
The joints of the lower extremities, especially the knee, ankle, and foot joints are the most common sites of involvement, but the wrist and fingers can be involved as well

14. CLINICAL FEATURES
The arthritis is usually quite painful, and tense joint effusions are not uncommon, especially in the knee
Dactylitis, or "sausage digit”
Tendinitis and fasciitis are particularly characteristic lesion:Achilles insertion, the plantar fascia
Spinal and low-back pain are quite common

19. CLINICAL FEATURES
Urogenital lesions: urethritis,Prostatitis cervicitis or salpingitis
Eye: conjunctivitis, anterior uveitis
Mucocutaneous lesions:Oral ulcers keratoderma blenorrhagica, circinate balanitis, Nail changes
Heart: cardiac conduction defects, aortic insufficiency

24. LABORATORY FINDINGS
ESR
CRP
HLA-B27

25. Imaging Soft tissue swelling.
Early disease:
Soft tissue swelling.
Reactive new bone formation, not joint erosion.
Linear periostitis and periosteal spurs

26. Imaging Spinal changes:
Asymmetric paravertebral ossification of lower thoracic and upper lumbar vertebrae.
Sacroiliitis is the single most important hallmark of Reiter’s and other spondyloarthropathies. Up to 70 % of chronic Reiter’s patients will show sacroiliac changes on lumbar spine examination

32. DIAGNOSIS ReA is a clinical diagnosis
No definitively diagnostic laboratory test or radiographic finding
The diagnosis should be entertained in any patient with an acute inflammatory, asymmetric, additive arthritis or tendinitis
Synovial fluid aspiration and analysis may be helpful in excluding septic or crystal-induced arthritis.

33. TREATMENT NSAIDs(Indomethacin 150mg) Doxycycline Minocycline
Corticosteroids
Sulfasalazine
MTX

34. Course
Long-term follow-up studies suggest that some joint symptoms persist in 30 to 60% of patients with ReA
Recurrences of the acute syndrome are common(25%)
Secondary AS